The major goal of this proposal is to elucidate for the first time the mode of action of a teratogen at the molecular level in both animal models and humans with congenital abnormalities. The abnormality to be studied is teratogen-induced cleft palate and the mechanism of action to be studied is the involvement of specific cytosol and nuclear receptor proteins in the corticoid induced derangement of gene action in mice. We propose to correlate the kind and amount of these receptors with the differing degree of teratogenic susceptibility to cleft palate by corticoids in different strains of mice. We also plan to determine whether other cleft palate teratogens have involvement of receptor proteins in their teratogenicity and whether these receptor proteins can be identified in children with cleft palate. Ultimately, we hope to be able to detect teratogenic vulnerability of human fetuses exposed to drugs by the receptor level in amniotic cells taken at amniocentesis.